Evidence map›Paper›PMID 25381825›Full record

ArticleOncogene2015

Coiled-coil domain containing 68 (CCDC68) demonstrates a tumor-suppressive role in pancreatic ductal adenocarcinoma.

N Radulovich, L Leung, E Ibrahimov, R Navab, S Sakashita, C-Q Zhu, E Kaufman, W W Lockwood, K L Thu, Y Fedyshyn and 3 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.4field-weighted citation impact, top 34% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 29 citations in OpenAlex.

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  16. Review
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  18. Overexpression of CCDC69 activates p14Journal of ovarian research · 2019
    Article
  19. Article
  20. Overexpression of Coiled-Coil Domain-Containing Protein 34 (CCDC34) and its Correlation with Angiogenesis in Esophageal Squamous Cell Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 1 country.

N Radulovich1] Princess Margaret Cancer Center, University Health Network, Toronto, ON, Canada [2] Department of Laboratory Medicine and Pathobiology Department, University of Toronto, Toronto, ON, Canada.
L Leung1] Princess Margaret Cancer Center, University Health Network, Toronto, ON, Canada [2] Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada.
E IbrahimovPrincess Margaret Cancer Center, University Health Network, Toronto, ON, Canada.
R NavabPrincess Margaret Cancer Center, University Health Network, Toronto, ON, Canada.
S SakashitaPrincess Margaret Cancer Center, University Health Network, Toronto, ON, Canada.
C-Q ZhuPrincess Margaret Cancer Center, University Health Network, Toronto, ON, Canada.
E KaufmanPrincess Margaret Cancer Center, University Health Network, Toronto, ON, Canada.
W W LockwoodBritish Columbia Cancer Research Centre and Department of Pathology, University of British Columbia, Vancouver, BC, Canada.
K L ThuBritish Columbia Cancer Research Centre and Department of Pathology, University of British Columbia, Vancouver, BC, Canada.
Y FedyshynDepartment of Molecular Genetics, Banting & Best Department of Medical Research, University of Toronto, Toronto, ON, Canada.
J MoffatDepartment of Molecular Genetics, Banting & Best Department of Medical Research, University of Toronto, Toronto, ON, Canada.
W L LamBritish Columbia Cancer Research Centre and Department of Pathology, University of British Columbia, Vancouver, BC, Canada.
M-S Tsao1] Princess Margaret Cancer Center, University Health Network, Toronto, ON, Canada [2] Department of Laboratory Medicine and Pathobiology Department, University of Toronto, Toronto, ON, Canada [3] Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada.
University Health Network · CAUniversity of British Columbia · CAPrincess Margaret Cancer Centre · CAUniversity of Toronto · CA

Funding

CIHR 137071-1CIHR 53912-1
6 · The paper itself

Abstract

Using integrative genomics and functional screening, we identified coiled-coil domain containing 68 (CCDC68) as a novel putative tumor suppressor gene (TSG) in pancreatic ductal adenocarcinoma (PDAC). CCDC68 allelic losses were documented in 48% of primary PDAC patient tumors, 50% of PDAC cell lines and 30% of primary patient derived xenografts. We also discovered a single nucleotide polymorphism (SNP) variant (SNP rs1344011) that leads to exon skipping and generation of an unstable protein isoform CCDC68Δ(69-114) in 31% of PDAC patients. Overexpression of full length CCDC68 (CCDC68(wt)) in PANC-1 and Hs.766T PDAC cell lines lacking CDCC68 expression decreased proliferation and tumorigenicity in scid mice. In contrast, the downregulation of endogenous CCDC68 in MIAPaca-2 cells increased tumor growth rate. These effects were not observed with the deletion-containing isoform, CCDC68Δ(69-114).

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCarcinoma, Pancreatic DuctalCell Line, TumorCell ProliferationHumansImmunohistochemistryIn Situ Hybridization, FluorescenceMice, SCIDMutationPancreatic NeoplasmsPolymorphism, Single NucleotideProtein IsoformsReverse Transcriptase Polymerase Chain ReactionRNA InterferenceTransplantation, HeterologousCCDC68 protein, humanProtein IsoformsTumor Suppressor Proteins

Identifiers

PMID25381825
PMCPMC5153324
OpenAlexW2079601616

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.